Anxiety has been associated with new-onset cardiovascular disease (CVD), but the quality of this relationship is unclear. Only if anxiety is a causal, independent cardiovascular risk factor might it be a target for CVD prevention.

Aims

To determine and examine the independent association and causality between anxiety and incident CVD.

Method

PubMed, EMBASE and PsycINFO databases were searched up to October 2013. A review of Hill's criteria for causality and random effects meta-analysis were conducted of prospective, population-based studies examining anxiety and incident CVD in people free from CVD at baseline.

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We read with interest the recent paper by Batelaan et al 1 evaluating the relationship between anxiety and cardiovascular disease at our weekly Journal Club. The authors found that anxiety is associated with a 52% increased incidence of CVD, that the relationship appeared to be causal, and independent of depression and traditional risk factors. Their definition of anxiety ranged from self-reported symptoms to post traumatic stress disorder. The magnitude of the association was similar to that of obesity. Their definition of anxiety ranged from self-reported symptoms to post traumatic stress disorder.

This is very important, as stress and anxiety are the leading cause of workplace absenteeism and do not receive the same level of attention at a government or societal level as obesity. If anxiety is indeed as potent a risk factor for CVD as obesity, one would hope that a comparable system level approach to its management, involving media campaigns, schools and workplaces, would naturally follow.

The authors stopped short of this recommendation, instead promoting further examination of the biological and behavioural underpinnings of their association, and in the meantime encouraging healthy life habits. While we recognise the importance of improved understanding of underlying mechanisms, surely, with the ready availability of effective treatments for anxiety at a primary prevention level (eg. Mindfulness, Positive Psychology), and secondary prevention level (eg. Psychotherapy, SSRIs), it might indeed be sensible to strongly encourage experimental studies, despite the challenge involved, particularly in view of the fact that this was identified as a gap in the knowledge on the area?

Another issue raised was the inclusion of PTSD in the study. PTSD has been associated with elevated basal heart rates and bood pressure 2. It has been moved from the Anxiety Disorders section to the Trauma and Stressor Related Disorders section in DSM V 3 and differs greatly in its biology from anxiety in terms of central noradrenergic effects and sympathoadrenal axis activity 4. The subgroup analysis in Batelaan et al’s study showed no differences between pooled hazard ratios in studies examining PTSD versus anxiety, however the proportion of positive studies was higher in the PTSD group (five out of six studies comprising a fifth of the overall population studied). If future efforts are to focus on biological underpinnings of the association between anxiety and CVD, it stands to reason that PTSD ought to be excluded.

1.Batelaan N, Seldenrijk A, Bot M, van Balkom A, Penninx B

Anxiety and new onset of cardiovascular disease: critical review and meta-analysis

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